New paper on hold

[Hustler]

This article has a delayed release (embargo) and will be available in PMC on December 1, 2017.
ENDOGENOUS RETROVIRUSES MOBILIZED DURING FRIEND MURINE LEUKEMIA VIRUS INFECTION
Stefano Boi, Kyle Rosenke, Ethan Hansen, Duncan Hendrick, Frank Malik, Leonard H. Evans
Virology. Author manuscript; available in PMC 2017 Dec 1.
Published in final edited form as: Virology. 2016 Dec; 499: 136–143. Published online 2016 Sep 19. doi: 10.1016/j.virol.2016.07.009
PMCID:
PMC5102782
Related Manuscript ID: NIHMS818248
Reason: This article has a delayed release (embargo) and will be available in PMC on December 1, 2017. An abstract of the article is available in PubMed, which may also have a link to the full text at the journal site.
URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102782/





All it takes is an SFFV 7C10 GP55 exogenous Mikovits like retrovirus to kick start the havoc

 

[Hustler]

Virology. 2016 Dec;499:136-143. doi: 10.1016/j.virol.2016.07.009. Epub 2016 Sep 19.
Endogenous retroviruses mobilized during friend murine leukemia virus infection.

Boi S1, Rosenke K1, Hansen E1, Hendrick D1, Malik F1, Evans LH2.
Author information
Abstract
We have demonstrated in a mouse model that infection with a retrovirus can lead not only to the generation of recombinants between exogenous and endogenous gammaretrovirus, but also to the mobilization of endogenous proviruses by pseudotyping entire polytropic proviral transcripts and facilitating their infectious spread to new cells. However, the frequency of this occurrence, the kinetics, and the identity of mobilized endogenous proviruses was unclear. Here we find that these mobilized transcripts are detected after only one day of infection. They predominate over recombinant polytropic virusesearly in infection, persist throughout the course of disease and are comprised of multiple different polytropic proviruses. Other endogenous retroviral elements such as intracisternal A particles (IAPs) were not detected. The integration of the endogenous transcripts into new cells could result in loss of transcriptional control and elevated expression which may facilitate pathogenesis, perhaps by contributing to the generation of polytropic recombinant viruses.
Published by Elsevier Inc.

KEYWORDS:
Endogenous; Mouse; Proviruses; Pseudotyping; Retroviruses
PMID: 27657834 PMCID: PMC5102782 [Available on 2017-12-01] DOI: 10.1016/j.virol.2016.07.009
[Indexed for MEDLINE]




OooooooopS ?!

 

[weyland]

It's been known for a while that infection mobilizes ERVs. This is part of Naviaux's acute cell danger response model. Activation of ERVs is thought to be an important part of potentiating immune response to other pathogens. (ref) Lipkin's finding of RVs in 85% of patients may have a lot to do with this.

I'm not sure how much relevance this specific study has to humans with ME. It's a study on mice with a mouse virus. I don't think humans can be infected with friend virus, correct me if I'm wrong.

 

[weyland]

All it takes is an SFFV 7C10 GP55 exogenous Mikovits like retrovirus to kick start the havoc

I'm not sure what you're trying to say here. 7C10 is an anti-gp55 monoclonal antibody used in lab assays.

 

[weyland]

So, help me out here. I got sick in 2014 and thankfully missed the entire XMRV fiasco. When you say "XMRV mikovits", you're referring to spleen focus-forming virus right? If so, is there evidence that SFFV is xenotropic? If not, you shouldn't call it XMRV and should call it SFFV so we know what you're talking about.

You believe then that ME is caused by SFFV infection? Do you base this solely on the finding that a percentage of patients make antibodies that can react with SFFV env protein, or is there other evidence to support this?

 

[Hustler]

There was no fiasco from Mikovits.
There was fiasco from a lot of people against her though.
She detected her HGRV, an xmrv-like MLV using the sffv 7c10 gp55 assay and HIV discovery classic retrovirology complementary methods.

Am in full remission on antiretrovirals.

The contamination, no detection, no association papers were insufficient and the Lipkin study was rigged.
And researchers are soaking up funds to study paths that will need to nowhere while their own kids rot away.
Instead of giving them raltegravir with viread or azt. If only they knew how their own parents were letting them down

 

[Hustler]

Mikovits explaining mouse retroviruses from 34m30s in
Starts at 34:30

Elite scientist

Negative authors were stripped of their retrovirology instinct and curiosity by Wessely,McClure and Coffin and many hopped on their train in full motion to get published in Retrovirology which Coffin is editor for. RETROVIROLOGY steam train. Publishingggggg poiiiints oh yeah just like Coffin.

Big crimes, impeccably engineered

Plain awful. Executed with finess

The ones who had the most to lose were Wessely(thinking yourself dead)+Coffin(said MLVs and mice safe for vaccine production)


LET IT RIP DOWN ON THEM NOW


GET READY FOR THE END GAME


And when it heats up let me use any language I want

I was ALWAYS RIGHT
AND SO WAS MIKOVITS

 

[weyland]

She detected her HGRV, an xmrv-like MLV using the sffv 7c10 gp55 assay and HIV discovery classic retrovirology complementary methods.

Can you link me to where these findings are discussed in detail? All I have seen is that she detected antibodies to the envelope protein of SFFV, and Lipkin reproduced these findings in his multicenter study. The problem with this being that whatever epitope these antibodies were binding to could be highly conserved across retroviruses, endogenous or exogenous. ERVs are very closely related to many GRVs. You will find HERV env proteins being expressed in people with infections from other viruses as well as cancer, MS, etc. due to transactivation or immune signalling as I mentioned above (ref).

 

[Hustler]

Her assay does not detect endogenous retroviruses
It only detects exogenous ones
It is validated

 

[garnet10]

I'm not sure what you're trying to say here. 7C10 is an anti-gp55 monoclonal antibody used in lab assays.

Weyland, it sounds like this lab assay (7C10 anti-gp55 monoclonal antibody) is only available to researchers?

 

[Hustler]

Weyland, it sounds like this lab assay (7C10 anti-gp55 monoclonal antibody) is only available to researchers?

Yes only available to researchers
There is no HERV cross reaction
Demonstrable and Validated assay

 

[weyland]

Weyland, it sounds like this lab assay (7C10 anti-gp55 monoclonal antibody) is only available to researchers?

Yes, as far as I can tell no commercial lab produces this clone for sale.

 

[weyland]

Yes only available to researchers
There is no HERV cross reaction
Demonstrable and Validated assay

That is completely false. De Meirleir demonstrated that 7C10 cross reacts with HERVs.

Immunochemical analyses of 12 ME gut biopsies probed for viral antigens showed that eight samples of the duodenum were immunoreactive to antibodies raised against HERV proteins (Figure 1A–D). In contrast, no immunoreactivity was observed in any of the control duodenum samples (Figure 1E–H, p=0.003 by Chi-square). Additional analysis was conducted using two anti-gammaretroviral antibodies: goat polyclonal IgG antibody raised against the Gag protein of murine leukemia virus (Figure 2A) and a rat monoclonal IgG1κ antibody (clone 7C10) raised against the Env protein of spleen focus forming virus (Figure 2B). The observed immunoreactivity was reproducibly consistent with the previous anti-HERV results, suggesting that the antigammaretroviral antibodies were cross-reactive with the HERV antigen(s). Additionally, the immunoreactivity was observed to co-localize (Figure 2C) in cells with an eccentric nucleus and granular inclusions (Figure 2D). Consistent with previous observations using antibodies to HERVs, no immunoreactivity was observed in the control biopsies using either anti-gammaretroviral antibody (Figure 2E–G). Matched stomach biopsies collected from ME cases and controls were also analyzed, but were consistently nonreactive when probed with the same anti-HERV and antigammaretroviral antibodies (data not shown).

 

[Hustler]

Weyland........
CheeeeeeKKKKKKKy

You know very very well that De Meirleir is not qualified enough to say that

And that he worked with Harvey Whittemore who was put in jail

 

[weyland]

You know very very well that De Meirleir is not qualified enough to say that

Immunoassays aren't exactly rocket science. I assume most biology undergrads would be qualified enough to do much of the work in that paper. It'd be one thing if the results were shocking and unexpected but they're not.

 

[Hustler]

With regards to De Meirleir's pretence :



This manuscript claims that SFFV antibodies cross react with human
endogenous retroviral proteins like HERV-K env
The only data in the paper using anti HERV protein antibodies is Fig 1, which shows that HERV-K env, HERV-K gag, HERV-FRD env and HERV-R env reactivity.
These are the only and last data showing any reactivity with HERV antibodies.

In Fig 2, they show reactivity using a rat monoclonal SFFV ENV and goat anti MLV gag used in the science paper. There is only one cell in which they show these
reactivity merge!!!. The rest of the paper is done only with anti SFFV Env

In the results the authors state that this suggests that the anti gammaretroviral antibodies were cross-reactive with the HERV antigens. No compelling evidence is given to support this statement is true. They then proceed to use only anti SFFV
as a marker for HERV antigen reactivity in the rest of the paper.

 

[weyland]

This manuscript claims that SFFV antibodies cross react with human
endogenous retroviral proteins like HERV-K env

That is what they demonstrated with the experiments, yes.

There is only one cell in which they show these
reactivity merge!!!. The rest of the paper is done only with anti SFFV Env

Yes. The point of the paper is that the reactivity is localized to pDC cells which are not the majority of cells present in the tissue samples, shown in the morphology slides.

In the results the authors state that this suggests that the anti gammaretroviral antibodies were cross-reactive with the HERV antigens. No compelling evidence is given to support this statement is true.

Actually it is. Using your vaunted complimentary techniques, they both sequenced the RNA in the samples as well as attempted to culture the samples in order to determine if an infectious MLV was present. The results of those efforts were inconsistent with the true presence of an infectious exogenous virus.

 

[Ron]

Why would this paper be embargoed till December? Any guesses.

 

[weyland]

Why would this paper be embargoed till December? Any guesses.

Not sure. You can read it now on sci-hub if you want. I honestly don't see much relevance to ME with this paper.

 

[Hustler]

Mikovits clearly says :


Lack of cross reactivity between Herv K and SFFV Env


Lane 1-4 = NP7 IP with 7C10
Blot with Indicated antibodies

Lane 5 and 6 = cell lysates


NP-7 - mouse line expressing lots of SFFV gp55

MCF-7 human breast line expressing HervK env

7C10 rat monoclonal Antibody against SFFV gp55



Same thing likely to happen in HIV Aids
(Endogenous and recombinant viruses activated by EXOGENOUS HIV-like) retroviruses


Experts who themselves have used sffv 7c10 GP55,55, extensively say it is unlikely there is crossreactivity


Weyland,nothing scientific at all in your arguments on this part of De Meirleir s paper which hijacks in part some of Judy's research and adds a really fake spin to it which is totally under the belt. Nobody else has dared defend De Meirleir on his sffv 7c10 gp assertions.
Harvey Whittemore hired De Meirleir.
Harvey Whittemore went to jail.
Lipkin was open about the Lipkin study being negative even before it was concluded. In the design phase even.
Pretenders pretending to care.
And they seem to have found a crowd in you